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Amyloid Fibrils

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Related Experiment Video

Updated: Sep 6, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Microbiome Impact on Amyloidogenesis.

Jofre Seira Curto¹, Amat Surroca Lopez¹, Maria Casals Sanchez¹

¹Self-organization in Biological Systems Lab, Department of Biochemistry and Molecular Biology, Biosciences Faculty, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Spain.

Frontiers in Molecular Biosciences

|July 5, 2022

Summary

This summary is machine-generated.

Microbial amyloid proteins may interact with human proteins, potentially contributing to neurodegeneration. Understanding this microbiome-host crosstalk could lead to novel therapeutic strategies for neurological diseases.

Keywords:

amyloid bacteria gut microbiome neurodegenerative disease prion probiotic

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Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Area of Science:

Microbiology
Neuroscience
Biochemistry

Background:

The human microbiome comprises over 1,000 bacterial species, significantly outnumbering human genes.
Alterations in the gut microbiota have been increasingly linked to neurodegenerative diseases over the past decade.
Emerging evidence suggests microbial amyloid structures may initiate host protein aggregation.

Purpose of the Study:

To review existing evidence on the potential crosstalk between microbial and human amyloid proteins.
To explore the implications of this interaction in the context of neurodegeneration.
To highlight the therapeutic potential arising from understanding these mechanisms.

Main Methods:

Literature review of studies investigating microbial and human amyloid formation.
Analysis of research on the gut-brain axis and neuroinflammation.
Synthesis of evidence linking microbial components to host proteinopathies.

Main Results:

Evidence supports the feasibility of crosstalk between microbial and human amyloid proteins.
Microbial amyloids are widespread and persist in the body, posing a potential risk.
The sheer number and longevity of microbes amplify concerns regarding amyloid interactions.

Conclusions:

The interaction between microbial and human amyloid proteins is a plausible and potentially common factor in neurodegeneration.
Identifying specific microbes and their mechanisms is crucial for therapeutic development.
Targeting microbiome-host amyloid interactions offers a promising avenue for novel neurodegenerative disease therapies.